Oxytocin stimulates glucagon and insulin secretion in fetal and neonatal sheep

In adults of several species arginine vasopressin (AVP) and oxytocin (OT) stimulate pancreatic secretion of immunoreactive plasma glucagon (IRG). In fetal sheep AVP is an important stress hormone and may be simultaneously secreted with OT; however, their effects on IRG secretion are not known. We sought to determine if AVP and/or OT affected pancreatic IRG secretion in fetal and neonatal sheep. Either AVP or OT was infused for 30 min in chronically catheterized fetal and neonatal sheep, obtaining peripheral arterial and/or portal venous blood samples before; 10, 15, and 30 min during; and 15, 30, and 60 min after infusion for measurements of blood gases, hematocrit, IRG, immunoreactive plasma insulin (IRI) and plasma glucose. AVP did not affect IRG or IRI in fetal sheep (mean +/- SE, 133 +/- 1 days gestation), but small increases occurred in portal venous blood of lambs (2-49 days old). In contrast, OT (4.6 +/- 0.3 mU/min.kg; n = 12) increased fetal plasma IRG from 72 +/- 5 to 86 +/- 6 and 97 +/- 7 pg/ml (P less than 0.001) and IRI from 16 +/- 2 to 20 +/- 3 and 20 +/- 2 microU/ml (P less than 0.02) at 15 and 30 min, respectively; 157 +/- 11 microU OT/min.kg had no effect. In lambs (2-49 days old), 3.0 mU OT/min.kg increased arterial (n = 15) IRG from 139 +/- 19 to 367 +/- 43 and 483 +/- 76 pg/ml (P less than 0.01) and portal IRG (n = 8) from 167 +/- 39 to 341 +/- 72 and 502 +/- 148 pg/ml (P less than 0.01), respectively. Arterial and portal IRI also rose (P less than 0.01) from 36 +/- 4 to 82 +/- 12 and 105 +/- 32 microU/ml and from 29 +/- 5 to 65 +/- 13 and 51 +/- 7 microU/ml, respectively. Glucose was unchanged in all experiments. In fetal and neonatal sheep, AVP has minimal effects on IRG and IRI release. In contrast, OT increases both substantially; furthermore, there is a difference in fetal and neonatal responsiveness. OT may be important in modulating glucagon and insulin secretion during and after parturition.     

Effect of age on fasting plasma levels of pancreatic hormones in man.

The effect of age and adiposity on fasting plasma levels of pancreatic polypeptide (HPP), glucagon (IRG), insulin (IRI) and glucose was examined in 263 healthy subjects between the ages of 20-69 yr. Mean plasma levels of hPP rose continuously from the third through the seventh decades. Mean plasma levels of IRG rose within the third and fourth decades but failed to rise further thereafter. Mean plasma levels of IRI did not change with age. Mean plasma levels of glucose rose by approximately 2 mg/dl . decade. The correlations of age with hPP, IRG, glucose, and adiposity were 0.47, 0.35, 0.25 (all P less than 0.01) and 0.15 (P less than 0.05), respectively. When adjustments were made for adiposity, the correlations of age with hPP, IRG, and glucose remained. Adiposity correlated with IRI, IRG, and glucose but when age correction was made, only the correlation of adiposity with IRI persisted. We conclude that: 1) age has a significant effect on fasting plasma levels of hPP and IRG; 2) the patterns of the age-related changes in hPP and IRG are not the same, suggesting that there are differences in the mechanism(s) by which age influences plasma levels of these two pancreatic hormones; and 3) age should be considered in the interpretation of fasting plasma levels of hPP and IRG.     

Truncal vagotomy abolishes the somatostatin response to insulin-induced hypoglycemia in man

The mechanism whereby insulin-induced hypoglycemia stimulates release of immunoreactive somatostatin (SRIF-LI) into the peripheral circulation in man is unknown. We have measured the plasma SRIF-LI response to insulin-induced hypoglycemia in 16 healthy subjects and five subjects with prior truncal vagotomy. Mean nadir of plasma glucose was similar in the two groups (37 +/- 5 and 34 +/- 2 mg/dl in the control group). Hypoglycemia induced a brisk rise in plasma pancreatic polypeptide (hPP) concentrations in healthy subjects (maximum concentration 1563 +/- 245 pg/ml) whereas in none of the postvagotomy subjects was there a significant change in hPP concentrations, indicative of completeness of the truncal vagotomy. In healthy subjects SRIF-LI concentrations rose for a basal of 168 +/- 19 pg/ml to a maximum of 254 +/- 30 at 39 +/- 4 minutes (p less than 0.005) with an incremental area of 2.8 +/- 1 ng . min/ml above basel. In vagotomized subjects, the mean basal SRIF-LI concentration of 166 +/- 22 pg/ml was not significantly different from that in healthy subjects. After insulin injection, SRIF-LI concentration fell with a net decrement of -3.2 +/- 1 ng . min /ml below the basal. It is concluded that the SRIF-LI response to insulin-induced hypoglycemia is dependent upon vagal integrity. Section of the vagus unmasks a suppressive effect of insulin action or its metabolic or hormonal consequences on the concentration of SRIF-LI in plasma.     

Insulin-producing islet cell tumors

The types of islet cell pathology and the history and clinical course are presented for 82 patients with proven islet B-cell disease with hyperinsulinism. They form the basis for the recognition of the patient suspected of harboring this syndrome. Among laboratory tests and procedures for recognition of inappropriate hyperinsulinism, the evaluation of plasma levels of glucose (G) and immunoreactive insulin (IRI) on fasting is the most important, with calculation of the IRI/G ratio, if necessary. The determination of the concentration of basal proinsulin and C-peptide is also helpful. Suppression tests and provocative tests are used infrequently. Attempts at preoperative localization are recommended. Ultrasonography and arteriography are helpful, while transhepatic percutaneous portal venous sampling is the only procedure that can differentiate localized (solitary insulinoma) from diffuse hyperinsulinism caused by adenomatosis, hyperplasia, and nesidioblastosis (present in 18% of our patients). Intraoperative ultrasonographic localization may visualize nonpalpable tumors and exclude multiple tumors. Treatment of benign B-cell disease is primarily surgical, but a variety of drugs may be useful for temporary or more prolonged therapy.     

Progressive hepatocytic fatty infiltration in rats with prehepatic portal hypertension

BACKGROUND/AIMS: Homogenous evolution, with a narrow range of portal hypertension, degree of portosystemic shunt and hepatic atrophy has been described in the experimental model of prehepatic portal hypertension in the rat. However the great differences observed in the rats' liver weight could be attributed to a pathological alteration of the liver. Based on this, we performed an evolutive histological study of the liver. This study shows the existence of a progressive hepatocytic fatty infiltration. METHODOLOGY: Male Wistar rats with portal hypertension induced by triple stenosing ligation of the portal vein at 1 month (group II, n=4) and at 1 year (group IV, n=10) of postoperative evolution were used. The portal pressure, body, liver and splenic weights, types of collateral circulation and degree of mesenteric venous congestion were studied. The intracytoplasmatic lipid microvacuoles were quantified in hepatocytes with an image analyzer (software MIP/CID, Spain). The results were compared with those obtained in control rats with the same evolutive periods (Groups I and III). RESULTS: The hepatic fatty infiltration in Group II (TPVS 1 month) (30.12+/-53.92 micron2) is similar to that presented by Group III (Control 1 year) (16.52+/-45.20 micron2), while there is an increase (p<0.001) in Group IV (triple portal vein stenosis 1 year) (182.03+/-371.42 micron2) in relation to the other groups studied. The progressive hepatic fatty infiltration in triple portal vein stenosis rats is associated with a decrease of portal pressure and of the incidence of liver hepatic atrophy, portosystemic collateral circulation and mesenteric venous congestion. CONCLUSIONS: TPVS produces progressive hepatocytic fatty infiltration in the rat so that this prehepatic portal hypertension experimental model could also be considered as a hepatic steatosis model.     

The mechanism of vagal nerve stimulation of glucagon and insulin secretion in the dog

The mechanism of vagal nerve stimulation of glucagon (IRG) and insulin (IRI) secretion was investigated in halothane-anesthetized dogs. Both ventral and dorsal branches of the thoracic vagi were stimulated electrically (10 Hz, 5 msec, 13.5 mA, 10 min) below the heart. Arterial and superior pancreaticoduodenal venous plasma were sampled, superior pancreaticoduodenal venous plasma flow was measured, and net pancreatic output of IRG and IRI were calculated. During vagal nerve stimulation (n = 15) net pancreatic output of IRG doubled (delta = +0.83 +/- 0.28 ng/min, P less than 0.01; baseline = 0.81 +/- 0.15 ng/ min) and IRI quadrupled (delta = +3.5 +/- 1.5 mU/min, P less than 0.025; baseline = 1.1 +/- 0.3 mU/min). Arterial glucose levels increased by 7 +/- 2 mg/dl from 108 +/- 3 mg/dl (P less than 0.005). After atropine pretreatment (n = 7), the pancreatic IRI response to vagal nerve stimulation was +0.71 +/- 0.28 mU/min (P less than 0.025), a reduction of 80%. In contrast, atropine pretreatment changed neither the IRG response (delta = +0.87 +/- 0.36 ng/min; P less than 0.05) nor the arterial glucose response (delta = +9 +/- 3 mg/dl; P less than 0.025) to vagal nerve stimulation. Hexamethonium pretreatment (n = 9) abolished the pancreatic IRG response (delta = +0.13 +/- 0.11 ng/min; NS), the arterial glucose response (delta = +0.5 +/- 1.9 mg/dl; NS) and the pancreatic IRI response (delta = +0.16 +/- 0.31 mU/min; NS) to vagal nerve stimulation. It is concluded that vagal nerve stimulation in the dog produces a moderate increase of IRG secretion, mediated by a nonmuscarinic (peptidergic?) mechanism, and a marked increase of IRI secretion, mediated by a muscarinic mechanism. Both responses are dependent on nicotinic transmission.     

Pancreatic endocrine responses to nutrients and bombesin after segmental pancreas autotransplantation in dogs

The capacity of autotransplanted (ATP) distal pancreas segments with systemic venous and peritoneal exocrine drainage to support physiologic control of plasma glucose levels was tested, and compared with the functions of "simulated autotransplants" (SATP) prepared with similar dissection and peritoneal exocrine drainage, but with hepatic portal venous drainage, in dogs. In ATP in the postabsorptive state, plasma levels of glucose, immunoreactive insulin (IRI) and immunoreactive glucagon (IRG1) were normal. Autotransplants resulted in impaired glucose tolerance after meals with impaired early insulin responses, and the normal brisk rise of IRG1 in the plasma was delayed and reduced through the first 30 min of feeding. In ATP, also, the response to bombesin was abnormal; the normal stimulation of release of both IRI and IRG1 was delayed in both cases. In studies of responses to oral and intravenous glucose in ATP and SATP dogs, similar mild degrees of glucose intolerance were found with both routes of administration; however, whereas in ATP dogs increases of IRI were highly exaggerated with both routes of administration of glucose, in SATP dogs plasma IRI rose from subnormal levels in the postabsorptive state through subnormal increments with both routes of administration. Further studies are necessary to determine the relative importance of denervation and reduction of the mass of the pancreas in these effects, and to assess the significance of the differences in blood insulin levels in the two preparations.     

The gastrocolic trunk of Henle in pancreatic surgery: an anatomo-clinical study

From 37 peroperative and cadaver anatomical investigations, it was concluded that, in contrast to the information in common texts on anatomy and surgery, a venous gastrocolic trunk was observed in only 46% of subjects; a true bipod gastrocolic trunk of Henle was a rare (8%) phenomenon. In this respect, a variate venous anatomy at the inferior border of the neck of the pancreas, as observed in this study, must be taken into account during pancreatic surgery and radiological procedures in the pancreas.     

Effects of long-term glibenclamide administration on gastrointestinal and pancreatic hormones in normal fasting rats

We previously reported that sulfonylurea treatment reduces insulin (IRI), glucagon (IRG) and somatostatin (SRIF) release following metabolic stimuli from the isolated perfused pancreas of normal rats and that a reduction in IRI, IRG and SRIF pancreatic content was also observed. The present work was undertaken to investigate the effects of long-term glibenclamide treatment on the gastrointestinal content of gut hormones in normal rats. Moreover, the effects of sulfonylurea treatment on IRI, IRG, and SRIF pancreatic content were also analyzed and compared to the peripheral hormone plasma levels. Two groups of male Sprague-Dawley rats received glibenclamide (1 mg/kg/day per os; n = 14) or placebo (distilled water; n = 10) for 5 months, respectively. Tissue contents of IRI, IRG and SRIF in acid-ethanol extracts of pancreas and of gastric inhibitory peptide (GIP), vasoactive intestinal polypeptide (VIP), entero-glucagon (gut-GLI) and SRIF in acid-ethanol extracts of intestine were determined. Blood glucose and plasma pancreatic hormone levels were also measured. Glibenclamide treatment lowered the levels of IRI, IRG and SRIF in the pancreatic tissue; in the same way gut-GLI, SRIF and VIP intestinal concentrations were significantly reduced, whereas no significant inhibition was detected in intestinal GIP content. Blood glucose levels and IRI and SRIF plasma concentrations were similar in the two groups. IRG plasma levels were reduced in the sulfonylurea group. These findings might suggest that sulfonylurea suppresses hormone biosynthesis in a non-specific manner.     

Total pancreatectomy with segmental duodenectomy preserving right gastroepiploic vein

We performed total pancreatectomy with segmental duodenectomy preserving the gastrocolic trunk and right gastroepiploic vein, to prevent gastric venous congestion, for treatment of pancreatic tumor. This is believed to be the first report of such a procedure. The patient was a 58-year-old man with high serum levels of carbohydrate antigen 19-9 and carcinoembryonic antigen. He was examined by abdominal ultrasonography and computed tomography, and diagnosed with cancer of the pancreatic body. No distant metastasis was found. We decided to perform distal pancreatectomy. After surgery, the cut edge of the distal pancreas was subjected to frozen section examination, and there was carcinoma in situ in the stump of the main pancreatic duct. Therefore, we cut the pancreatic head partially, twice, but carcinoma in situ remained. We additionally performed pancreatic head resection with segmental duodenectomy, with preservation of the gastroduodenal artery, right gastroepiploic artery, gastrocolic trunk and right gastroepiploic vein to prevent gastric venous congestion. The postoperative course was uneventful and the patient remains in good condition. This surgical technique is considered feasible and safe for prevention of gastric venous congestion.     

Role of glucagon in hyperglycemic response during a short period of hemorrhage in anesthetized dogs

A role of pancreatic glucagon in hemorrhage induced hyperglycemia was studied in anesthetized dogs with or without functional adrenalectomy (ADRX), surgical hepatic denervation (HNX), and surgical pancreatectomy (PCX). Plasma epinephrine, norepinephrine, and glucose concentrations were determined in both hepatic venous and aortic blood. Plasma glucagon (IRG) and insulin (IRI) levels were determined in aortic blood. All dogs were bled until aortic systolic pressure dropped to approximately 50% (64.8 +/- 1.6 mmHg, n = 25) of its control value (136.7 +/- 4.4 mmHg, n = 25), and the hypotension was maintained for 5 min. In control dogs (n = 10), hemorrhage markedly increased aortic epinephrine and hepatic venous norepinephrine. Similarly, aortic IRG, hepatic venous glucose and aortic glucose rose significantly during hemorrhage. In dogs with HNX combined with ADRX (n = 10), aortic epinephrine and hepatic venous norepinephrine remained unchanged during hemorrhage. Aortic IRG concentration, however, increased to a level similar to that observed in the control group. Aortic glucose increased significantly along with significant increases in hepatic venous glucose. In dogs with PCX combined with HNX and ADRX (n = 5), the increases in aortic IRG, hepatic venous glucose and aortic glucose observed in the first two groups in response to hemorrhage were virtually abolished. The results indicate that the increase in aortic IRG during hemorrhage is of pancreatic origin. We conclude that the pancreatic glucagon may be involved in the hyperglycemic response to hemorrhage, most likely through glucose mobilization by the liver during the early phase of hemorrhagic hypotension.     

Venous anatomy of the right colon: precise structure of the major veins and gastrocolic trunk in 58 cadavers

PURPOSE: This study was designed to describe the precise venous anatomy of the right colon, which is especially important for laparoscopic right hemicolectomy. METHODS: Fifty-eight adult cadavers were dissected to define the three major venous tributaries of the right colon: the ileocolic vein, right colic vein, and middle colic vein. Two or three middle colic veins were often present, and the biggest one was designated as the main middle colic vein. The middle colic vein and the right colic vein occasionally formed a common trunk with the right gastroepiploic vein and/or the pancreaticoduodenal vein. This common trunk was defined as the gastrocolic trunk. RESULTS: All 58 cadavers had a single ileocolic vein. All of the ileocolic veins drained into the superior mesenteric vein. The right colic vein was absent in 56.9 percent (33/58), and the other 43.1 percent had a single right colic vein. The right colic vein joined the superior mesenteric vein directly in 56 percent (14/25) and the gastrocolic trunk in 44 percent (11/25). The middle colic vein was the most variable. A single middle colic vein was present in 37.9 percent (22/58), 2 middle colic veins were present in 50 percent (29/58), and 3 middle colic veins were present in 12.1 percent (7/58). The main middle colic vein drained into the superior mesenteric vein directly in 84.5 percent (49/58), whereas 12.1 percent (7/58) drained into the gastrocolic trunk. In two cadavers, there was anomalous drainage of the main middle colic vein to the splenic vein and the inferior mesenteric vein. Forty-three accessory middle colic veins were present in total. These drained into the superior mesenteric vein in 17 cadavers and into the gastrocolic trunk in 23. The gastrocolic trunk was present in 69 percent (40/58), being formed with the right colic vein in 27.5 percent (11/40; 1 was together with an accessory middle colic vein) and with the middle colic vein in 75 percent (30/40; 7 with the main middle colic vein, 23 with the accessory middle colic vein). CONCLUSION: Venous anatomy of the right colon is highly variable. It is especially important to recognize the lack of direct drainage of the right colic vein to the superior mesenteric vein and the high frequency of the presence of plural middle colic veins and the gastrocolic trunk.     

Localization of islet-cell hyperplasia: value of pre- and intraoperative arterial stimulation and venous sampling

Arterial stimulation and venous sampling was effective in the localization of β‐cell hyperplasia of the pancreas in the islets of Langerhans in an 84‐year‐old woman. The patient presented with repeated episodes of unconsciousness and hypoglycemia. She was first suspected of having insulinoma, but diagnostic imaging failed to reveal any tumors. Arterial stimulation and venous sampling (ASVS) and percutaneous transhepatic portal venous sampling (PTPS) were performed to localize the tumor. By ASVS, increases in immuno reactive insulin (IRI) were noted in renal vein blood samples (because a splenorenal shunt was present) after splenic arterial stimulation and venous sampling, and PTPS revealed a stepup in IRI from splenic venous blood samples. Preoperative diagnosis suggested β‐cell hyperplasia in the pancreas tail. Intraoperative ultrasound failed to find a tumor. Intraoperative ASVS showed the site of increase IRI as the pancreas tail, so distal pancreatectomy and splenectomy were performed. However, hypoglycemia was observed constantly after this operation. Relaparotomy, causing additional resection, was conducted to confirm the precise location and to remove the residual β‐cell hyperplasia of the pancreas. At the second resection, the existing part of β‐cell hyperplasia was confirmed through intraoperative ASVS, and additional resection of the pancreas body and neck was performed. At this time, complete removal of the residual β‐cell hyperplasia was confirmed through ASVS. The hypoglycemia and impaired consciousness disappeared after the operation, and the patient's blood sugar level was maintained at a normal level. Pathological findings revealed islets of Langerhans hyperplasia extending to 1 cm in the pancreas tail region. We conclude that pre‐ and intraoperative ASVS is a useful test for β‐cell hyperplasia, which is difficult to diagnose through ordinary imaging techniques.     

Disopyramide induces insulin secretion and plasma glucose diminution: studies using the in situ canine pancreas

The mechanism of disopyramide-induced hypoglycemia, a life-threatening complication in the antiarrhythmic drug treatment, is still controversial. To elucidate this, we have evaluated plasma insulin (IRI) and glucagon (IRG) responses in the pancreatic vein (PV) of the in situ pancreas as well as responses of plasma IRI, IRG, and glucose in the femoral artery (FA) to disopyramide phosphate administration in anesthetized dogs. First, infusion of disopyramide at a dose of 50 mg for ten minutes directly into the pancreatic artery, but not the vehicle, increased significantly plasma IRI concentration in the PV (P less than .05 or less), where the IRI response started within three minutes and reached a peak of 2.8-fold preinfusion value at 30 minutes after starting the infusion (n = 7). Plasma IRI concentration in the FA also increased slightly but significantly (P less than .05). Plasma IRG concentration in the PV initially decreased significantly (P less than .05 or less) and in the FA at one point (P less than .05) during the infusion, and then increased significantly after cessation of the infusion, showing a peak of 1.9-fold preinfusion value at 60 minutes in the PV and the FA (P less than .05). Plasma glucose concentration in the FA decreased slowly and significantly after the infusion (P less than .05 or less) and fell by 16% of the baseline value at 60 minutes (P less than .05). Second, serum disopyramide concentration of 13.7 +/- 2.8 micrograms/mL at ten minutes, which corresponds to a twofold to threefold concentration of the human therapeutic level (n = 4).(ABSTRACT TRUNCATED AT 250 WORDS)     

Glucoregulation in alloxan-diabetic dogs

In order to establish whether a prolonged subnormal secretion of insulin may affect glucoregulation against hypoglycemic stimuli, the level of plasma glucose was decreased in alloxan-diabetic dogs by the infusion of either 50 micrograms/kg . min phlorizin (PHL), ie, reducing the concentration of plasma glucose without hyperinsulinemia; or with 7 mU/kg . min insulin (combined hyperinsulinemia and hypoglycemia). The concentration of glucose, immunoreactive glucagon (IRG), and insulin (IRI) and catecholamines were followed in the plasma. Hepatic glucose production (Ra) and the overall rate of glucose removal from the circulation were calculated by a tracer method. During a 200-minute infusion of PHL plasma glucose fell from 328 +/- 29 to 114 +/- 16 mg/dl, while IRG rose from a mean of 470 +/- 123 to 623 +/- 200 pg/mL, however this increase was significant only in 3 out of 6 dogs. There was no change in the plasma level of epinephrine. Plasma IRI decreased significantly, the IRI/IRG ratio remained low, and Ra did not increase. When the animals were treated with insulin for one week, plasma glucose was restored to normal, while plasma IRI and the IRI/IRG ratio were raised above the normal level. Under these circumstances the infusion of PHL increased plasma IRG significantly from 59 +/- 5 to 110 +/- 32 pg/mL, decreased IRI slightly, and increased Ra by an average of 50 +/- 16%. No measurable change in plasma glucose was observed indicating the restoration of nonhypoglycemic glucoregulation. In diabetic dogs during a 95-minute infusion of insulin, plasma glucose dropped from a mean of 338 +/- 5 to 74 +/- 24 mg/dL.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pancreatic head tumors with portal vein involvement: an alternative surgical approach.

BACKGROUND/AIMS: One of the determining factors for the unresectability of pancreatic head tumors is the involvement of the portal venous system. Recent reports show that the resection of tumors with portal vein involvement has similar results to lesions with same stage without portal vein invasion. The aim of this study is to present a technique that allows the resection of portal vein segments without the use of grafts and with a shorter period of intraoperative venous occlusion. METHODOLOGY: Fifteen patients with pancreatic head tumors and portal vein involvement were submitted to pancreaticoduodenectomy according to this technique. The main feature of the technique is starting the pancreatic dissection at the posterior aspect of the head of the pancreas. The superior mesenteric artery is completely dissected from the pancreatic tissues leaving the section of the pancreas and the resection of the portal vein to the last step. RESULTS: Portal vein flow occlusion did not exceed 10 minutes. There were no major postoperative complications or mortality. CONCLUSIONS: This maneuver allows an easier resection of the mobilized portal vein with a shorter period of venous clamping and reconstruction without the need of venous graft.     

The role of insulin and glucagon in the plasma aminoacid imbalance of chronic hepatic encephalopathy.

Increased glucagon (IRG) levels have been documented in liver cirrhosis, particularly associated with portal-systemic shunting. In spite of increased insulin (IRI) levels, IRI/IRG are reduced. This alteration has been proposed to have a pathogenic role in plasma aminoacid imbalance which seems to account for hepatic encephalopathy. We studied IRG and IRI/IRG in 13 controls and in 3 groups of cirrhotics, divided on the basis of their mental state. Glucagon was determined by means of 30 K Unger's antibody; insulin by a double antibody technique. Results are expressed in the table as means +/- SEM. (Formula: see text)A progressive increase in IRG secretion is present in cirrhotics and correlates with the mental state; IRI/IRG is not altered in cirrhosis until neurological distrubances are present. A relative fall in IRI which can no more balance the increasing IRG values characterizes hepatic encephalopathy.     

Subcutaneous, isogeneic transplantation of duct-ligated pancreas in streptozotocin diabetic mice: relationships between recovery and hormone contents in transplants or host pancreas.

Recovery from diabetes was observed in streptozotocin-treated mice that received subcutaneous, isogeneic transplants of duct-ligated pancreas. Transplants excised from recovered hosts contained both immunoreactive insulin (IRI) and glucagon (IRG), indicating that both A and B cells capable of hormone storage were present. The IRI content in transplants, although only one sixth of that transplanted 6 wk earlier, was still 21/2 times greater than that in the host pancreas and was inversely related to the plasma glucose of the recipient during and after recovery. The IRI content in the transplant added to that in the host pancreas totaled 13% of the IRI found in the normal mouse pancreas, which sufficed for over-all recovery from diabetes but was insufficient to provide normal glucose tolerance and insulin response to a major glucose challenge. The abnormally high content of glucagon noted in the pancreas of hyperglycemic, sham transplanted mice was reduced by one-half in the pancreas of those transplanted mice returning to normal plasma glucose and insulin. Thus, the insulin content of the transplant was important to the recovery of isografted mice, but in addition, and perhaps as a consequence of recovery, there was a slight increase in the insulin storage capacity of the host pancreas and a marked reduction of glucagon compared to the content of these hormones in the pancreas of hyperglycemic, sham transplanted mice.     

An anomaly in persistent right umbilical vein of portal vein diagnosed by ultrasonography

AIM: To detect the anomaly in the persistent right umbilical vein (PRUV) of portal vein (PV) with deviation of the ligamentum tere and left-sided gallbladder. METHODS: A total of 5783 candidates for routine analysis were evaluated for hepatic vascular abnormalities by ultrasonography. RESULTS: Ten candidates (0.17%) had a portal vein anomaly with a rightward-deviated ligamentum tere. The blood-flow velocity in the PRUV of the portal vein (17.7±3.0 cm/s) of the 10 cases was similar to that of the right anterior portal trunk (17.6±4.1 cm/s). However, the vessel diameter of the PRUV (φ12.4±4.4 mm) was larger than the right anterior portal trunk (φ6.1?.9 mm). Therefore, flow volume in the anomalous portion (0.97±0.30 L/min) was more than that in the right anterior portal trunk (0.18±0.05 L/min). CONCLUSION: The anomaly plays an important role in intra-hepatic PV flow.     

Metabolism of insulin and immunoreactive insulin-like substances (proinsulin, HWIRI) in vivo in man

Immunoreactive insulin (IRI) and its three constituents as determined by gel filtration: high molecular weight substances with insulin immunoreactivity (HWIRI), proinsulin (PI) and insulin (I), were measured hourly during 28 hours in the portal, hepatic and peripheral venous systems of a patient operated for a nesidioblastoma. The PI levels were constant from one system to the other (7.1 +/- 0.8 microU/ml; 7.3 +/- 0.8 microU/ml; 9.2 +/- 1.2 microU/ml). The I levels decreased from the portal (53.3 +/- 5.2 microU/ml) to the hepatic venous system (28.0 +/- 1.0 microU/ml) and from the latter to the peripheral venous system (19.8 +/- 2.0 microU/ml). The HWIRI levels were stable between the portal and the hepatic venous systems (4.7 +/- 0.7 microU/ml; 4.8 +/- 0.6 microU/ml) and higher in the peripheral system (8.2 +/- 1.2 microU/ml). Our results demonstrate that: --I is essentially degraded by the liver. --There is no variation of PI in the three compartments. --HWIRI is formed in the circulation. --Variations of IRI levels between venous systems acquire physiological significance only when accompanied by the variations of the levels of each constituent.